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Vol 54(2020) N 6 p. 884-893; DOI 10.1134/S0026893320060114 Full Text

D. Sun1, W.-Y. Li2, S.-H. Chen3, Z.-F. Zhi1, H.-S. Lin1, J.-T. Fan1*, Y.-J. Fan4**

shRNA-Mediated Suppression of γ-Synuclein Leading to Downregulation of p38/ERK/JNK Phosphorylation and Cell Cycle Arrest in Endometrial Cancer Cells

1Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021 People's Republic of China
2Department of Gynaecology and Obstetrics, Liuzhou General Hospital, Liuzhou, 545006 People's Republic of China
3Department of Gynaecology, Liuzhou Maternity and Child Healthcare Hospital, Liuzhou, 545001 People's Republic of China
4Department of Gynaecology and Obstetrics, University of Chinese Academy of Sciences, Shenzhen Hospital, Shenzhen, 518106 People's Republic of China

*yjfan530@163.com
**jiangtaofan1969@163.com
Received - 2019-11-23; Revised - 2020-03-18; Accepted - 2020-03-23

In this study, we explored the effects of treating human endometrial cancer cells with γ-synuclein-specific short hairpin RNA (shRNA) and elucidated the associated mechanisms in vitro and in vivo through the p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK) signaling pathways. Cell proliferation and migration were assessed using CCK8, Transwell, and scratch wound healing assays. Flow cytometry and laser scanning confocal microscopy were used to detect cell cycle changes. Relative levels of phosphorylated and non-phosphorylated (p) p38, ERK1/2 and JNK1/2/3 were determined in vitro and in vivo using simple western blotting assays. Cell proliferation in the experimental group decreased significantly and cells transfected with shRNA showed reduced migration rates (P < 0.05). p-p38, p-ERK1/2, and p-JNK1/2/3 levels were downregulated in the experimental group in vitro and in vivo. Tumor volumes and weights in the experimental group were significantly lower (P < 0.05). Tumor formation time in the negative control group was significantly shorter (P < 0.05). Flow cytometry showed that the number of cells in the G1 and mitotic phases increased and that in the S phase decreased after SNCG silencing (P < 0.05). Confocal microscopy showed that the percentage of cells in the mitotic phase increased after SNCG gene silencing (P < 0.05). We conclude that shRNA-mediated suppression of γ-synuclein decreased the proliferation, migration, and tumorigenicity of endometrial cancer cells via downregulation of p38, ERK, and JNK phosphorylation. High SNCG expression is closely related to the growth cycle of endometrial cancer cells.

γ-synuclein, SNCG, endometrial cancer, p38, ERK, JNK



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